Editor – In their lesson of the week article, Raja Shariff et al listed a differential diagnosis of Ortner’s syndrome which should have included not just compression of the left recurrent laryngeal nerve (LRLN) by left atrial enlargement but also compression of the recurrent laryngeal nerve by a ‘large thrombotic formation that completely occlude(s) the outflow tract of the pulmonary artery’, as in the case of pulmonary embolism (PE) reported by Polverino et al.1,2 Accordingly, for the sake of completeness, they should have evaluated their patient not only for left atrial enlargement but also for stigmata of PE.
The rationale for evaluation for PE even when left atrial enlargement has been documented by echocardiography is that mitral stenosis is a risk factor for PE (and, hence, for Ortner’s syndrome) in its own right, and also a risk factor for mitral stenosis-related mortality.3–5 The occurrence of mitral stenosis-related PE was exemplified by a 43-year-old man who presented with severe mitral stenosis, atrial fibrillation (AF) and haemoptysis. Contrast enhanced computed tomography demonstrated the presence of a left pulmonary embolism. Left atrial thrombus was also present, as shown by cardiac magnetic resonance imaging and by transthoracic echocardiography. Deep vein thrombosis was excluded by ultrasonography.3 In the clinicopathological study of 51 cases of mitral stenosis published by Jordan et al, pulmonary emboli or infarcts were present at necropsy in 27 cases. In that study, 16 of the instances of PE and/or pulmonary infarct were associated with the presence of mural thrombi in the right atrium. Furthermore, peripheral venous thrombi were found in eight cases.4 Pulmonary embolism was listed as a cause of death in six of the 59 patients with mitral stenosis-related mortality reported by Donzelot et al.5
PE-related Ortner’s syndrome has not been reported in the context of mitral stenosis. Nevertheless, in view of the above observations and in order to maximise the impact of ‘lesson of the week’ as a ‘teachable moment’, evaluation for PE should be included in the evaluation of mitral stenosis patients with vocal cord paralysis even when left atrial enlargement is present.2–5 The purpose of that exercise would be to rule out (or rule in) the possibility that LRLN compression might be attributable to mitral stenosis-related PE, given the fact that the latter can have a fatal outcome. At the very least, evaluation for PE should include an evaluation for peripheral venous thrombi (as a risk factor for PE) and a transoesophageal evaluation specifically to look for stigmata of PE.
References
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